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. 2021 Mar 17;91(1):73–82. doi: 10.1038/s41390-021-01457-y

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — In NEC patients or cells challenged by LPS, TLR4 is activated. On the one hand, TLR4 binds to TRIF to activate necroptosis. On the other hand, TLR4 activation induces the production of inflammatory cytokines including TNF-α, which further binds with TNFR1 and leads to apoptosis and necroptosis simultaneously. When RIPK1 is inhibited by necrostatin-1s, or when TLR4 is removed, necroptosis becomes suppressed. The production of TNF-α is also reduced so that caspase-8 is decreased, leading to a decreasing trend of apoptosis. Meanwhile, the suppression of RIPK1 might relieve its inhibitory effect on caspase-3, leading to an increased trend of apoptosis. These two effects may counteract each other, but in general necrostatin-1 and TLR4 knockout showed an alleviating effect on NEC mice.